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Laringomalacia congénita
AUTORES: Dra. Dana M. Thompson, MS, MBA, FACS, Dr. Taher Valika
EDITOR DE LA SECCIÓN: Glenn C. Isaacson, MD, FAAP
EDITOR ADJUNTO: Carrie Armsby, doctora en medicina y máster en salud pública

Todos los temas se actualizan a medida que hay nueva evidencia disponible y se completa nuestro proceso de revisión por
pares .

Revisión de literatura actualizada hasta: marzo de 2025.

Última actualización de este tema: 30 de enero de 2025.

INTRODUCCIÓN
La laringomalacia congénita es una de las causas más comunes de respiración ruidosa en
bebés. El estridor se ausculta durante la inspiración y se debe al prolapso del tejido supraglótico
hacia la entrada glótica ( vídeo 1 e imagen 1 ).

Aquí se revisarán las características clínicas, el diagnóstico y el tratamiento de la laringomalacia

congénita en lactantes y niños. La laringomalacia es distinta de la traqueomalacia (traquea
distensibilidad anormal), que es mucho menos frecuente. La traqueomalacia se analiza con más
detalle por separado. (Véase "Anomalías congénitas de las vías respiratorias intratorácicas y
fístula traqueoesofágica", sección sobre "Traqueomalacia" ).

Otras anomalías congénitas de la laringe (p. ej., hendiduras y membranas laríngeas) y otras
causas de estridor en lactantes y niños se analizan por separado. (Véase "Anomalías congénitas
de la laringe" y "Evaluación del estridor en niños" ).

EPIDEMIOLOGÍA
La laringomalacia congénita es la causa más común de estridor recurrente o crónico en la
infancia, y representa aproximadamente entre el 45 y el 75 por ciento de los casos remitidos a
clínicas especializadas de otorrinolaringología [ 1,2 ]. La prevalencia informada de
laringomalacia clínicamente significativa es de aproximadamente 3 a 4 casos por cada 10 000
nacidos vivos [ 3 ]. Es más común en hombres que en mujeres, con una proporción hombre-
mujer de aproximadamente 1,5:1 [ 2 ].

La laringomalacia puede presentarse en niños por lo demás sanos o puede estar asociada a
una afección médica subyacente (p. ej., síndrome genético, trastorno neuromuscular,
prematuridad). (Consulte "Afecciones asociadas" a continuación).

ANATOMÍA
● Anatomía laríngea normal : La laringe está compuesta de cartílago, músculos (extrínsecos e
intrínsecos) y un revestimiento mucoso ( figura 1 ). Los músculos de la laringe actúan para
abrir y cerrar la glotis y regular la calidad de la voz.

El hueso hioides, móvil y con forma de medialuna, forma el límite superior anterior de la
laringe. En los recién nacidos, la laringe se ubica a la altura de C3-C4; desciende
gradualmente a la altura de C6-C7 durante la adolescencia.

La laringe se divide en tres secciones según el nivel de las cuerdas vocales:

• Supraglottic structures – The area just above the vocal folds is called the supraglottic
region. The supraglottic structures include the epiglottis, arytenoids, aryepiglottic folds,
and false vocal folds.

• Glottis – This includes the vocal folds and the area just below the vocal folds.

• The subglottic region – This includes the region starting 1 cm below the vocal folds and
ending in the upper cervical trachea. It corresponds to the cricoid cartilage, which is the
only laryngeal cartilage that completely encircles the airway. It is the narrowest part of the
airway in infants and children.

● Anatomic classification of laryngomalacia – In infants and children with laryngomalacia,

supraglottic tissue collapses into the glottic inlet during inspiration.

The Olney classification schema categorizes laryngomalacia into three types based on
supraglottic morphology ( figure 2) [4]:

• Type 1 – Prolapse of redundant supra-arytenoid tissue

• Type 2 – Foreshortened aryepiglottic folds with an omega-shaped epiglottis ( picture 1
and movie 1)
• Type 3 – Retro-displaced epiglottis that collapses posteriorly during inspiration ( movie 2)
 Children with laryngomalacia can have anatomic findings that fit into a single category, or
they may have a combination of findings. In a systematic review of studies describing
characteristics of >1200 children with laryngomalacia, the relative frequency of the different
types was as follows [2]:

• Type 1 – 32 percent
• Type 2 – 47 percent
• Type 3 – 10 percent
• Combination of two or more types – 11 percent

A retro-displaced epiglottis (type 3 laryngomalacia) is most commonly seen in children with

underlying neurological disorders. (See 'Associated conditions' below.)

PATHOGENESIS
The pathogenesis of laryngomalacia is not fully understood. It likely results from a combination
of neurologic, anatomic, and inflammatory abnormalities leading to diminished tone of the
supraglottic tissue and supporting musculature [1,5,6].

Respiration, swallowing, and neuromuscular tone of the larynx are vagally mediated through
the laryngeal adductor reflex. The diminished airway tone and swallowing dysfunction seen in
laryngomalacia are thought to result from abnormal sensorimotor integration between
peripheral vagal nerve chemoreceptors and the central nuclei that control respiration and
swallowing via the laryngeal adductor reflex [1,7].

Anatomic factors (eg, redundant soft tissue in the supraglottis, foreshortened or tight
aryepiglottic fold) may also play a role. Another theory is that laryngomalacia results from
immature development of laryngeal cartilage [6].

Gastroesophageal reflux (GER) and laryngopharyngeal reflux (LPR) can be detected in most
patients with clinically significant laryngomalacia (see 'Associated conditions' below). GER and
LPR are thought to contribute to the pathogenesis of laryngomalacia by causing inflammation
of the already redundant supraglottic tissue. However, the role that GER and LPR play in the
pathogenesis of laryngomalacia is uncertain. The association between GER and laryngomalacia
may be explained by a common underlying mechanism (immature neuromuscular tone
affecting both the supraglottic airway and the lower esophageal sphincter) rather than a causal
relationship.
CLINICAL FEATURES
Presentation

Congenital laryngomalacia — Infants with congenital laryngomalacia may present primarily

with respiratory symptoms (eg, noisy breathing), feeding difficulties, or a combination of both
[8].

Most infants with congenital laryngomalacia present with noisy breathing that begins in the
newborn period. It may gradually become more noticeable over the first few months of life.
The stridor produced by laryngomalacia occurs during inspiration and can be intermittent.
(See 'Natural history' below.)

The stridor can occur at rest and tends to worsen with activities such as crying, agitation,
excitement, or feeding. Stridor is worse in the supine position and improves when the infant
is upright. The noise can have a "wet" quality which is often associated with concurrent reflux.
Stridor may be more pronounced during intercurrent respiratory illnesses, and some affected
children may be diagnosed with recurrent episodes of croup before the possibility of
laryngomalacia is suspected. (See "Croup: Clinical features, evaluation, and diagnosis", section
on 'Recurrent croup'.)

Expiratory stridor and hoarseness are not characteristic findings of laryngomalacia; these
findings should prompt consideration of an alternative diagnosis or secondary airway
abnormality. (See 'Differential diagnosis' below and 'Associated conditions' below.)

Infants and children with mild laryngomalacia feed well and have normal weight gain and
growth despite their noisy breathing. However, severe laryngomalacia can cause sleep-
disordered breathing, apneic/cyanotic episodes, severe feeding difficulties, and/or growth
failure [8,9]. In severely affected patients, suprasternal or substernal retractions may be
noted on examination ( movie 3). (See 'Severity assessment' below.)

In a single-center study of 324 infants and children laryngomalacia who were referred to a
specialty center for management, the relative frequency of symptoms was as follows [9]:

● Stridor – 93 percent
● Feeding difficulties – 50 percent
● Apnea – 19 percent
● Retractions – 18 percent
● Cyanosis – 13 percent
 ● Growth failure – 10 percent

Late presentation — Laryngomalacia presenting after infancy or early childhood is

uncommon in the absence of an underlying neuromuscular disorder or genetic syndrome.
However, late-onset variants of laryngomalacia have been described. Late presentations may
include [10,11]:

● Feeding variant – These patients typically present in the toddler years predominantly with
symptoms of swallowing dysfunction and feeding difficulties.

● Sleep variant – These patients typically present at school age with sleep-disordered
breathing (eg, persistent obstructive sleep apnea despite adenotonsillectomy). Often, a
detailed history will reveal a history of mild stridor in infancy that was not severe enough to
warrant intervention.

● Exercise variant – These patients typically present in later childhood or adolescence with
exercise-induced inspiratory stridor.

Patients with these late-onset variants usually have profound arytenoid redundancy and
prolapse noted on laryngoscopy but other typical anatomic features of congenital
laryngomalacia (shortened aryepiglottic folds, retroflexed epiglottis) may be absent [11].

Late-onset variants are rare, and the management of these patients is beyond the scope of
this topic.

Associated conditions — Comorbid medical conditions are common in infants and children
with congenital laryngomalacia.

● Gastroesophageal reflux (GER) – GER and laryngopharyngeal reflux (LPR) can be detected in
50 to 90 percent patients with clinically significant laryngomalacia [2,12-16]. GER and LPR are
thought to contribute to the pathogenesis of laryngomalacia by causing inflammation of the
already redundant supraglottic tissue (see 'Pathogenesis' above). In addition, the negative
intrathoracic pressure generated by recurrent episodes of airway obstruction can further
promote reflux of gastric contents, resulting in a vicious cycle that exacerbates symptoms of
both GER and airway obstruction.

If the supraglottic tissues are exposed to refluxed gastric contents recurrently over a
prolonged time, it may cause neuroinflammatory changes that alter laryngeal sensation and
tone [1]. This may lead to swallowing dysfunction, difficulty clearing secretions, and noisy
breathing that has a "wet" quality.
 Acid suppression therapy is commonly used in the management of laryngomalacia with the
rationale that it may reduce the adverse effects of GER and LPR in this setting. However,
based on the available evidence, it is unclear if acid suppression therapy improves symptoms
or reduces the need for surgical intervention in infants and children with laryngomalacia
[17,18]. Nevertheless, it remains the mainstay of medical management, as discussed below.
(See 'Initial interventions (medical therapy)' below.)

● Neuromuscular disorders – Laryngomalacia is common in children with neuromuscular

disorders such as cerebral palsy, hydrocephalus, Chiari malformation, myelomeningocele,
muscular dystrophy, or congenital hypotonia [1,19]. Children with an underlying
neuromuscular cause of laryngomalacia often also have significant swallowing dysfunction.

Laryngomalacia tends to be more severe and persistent in children with underlying

neuromuscular disorders compared with infants with isolated laryngomalacia who are
otherwise healthy. (See 'Natural history' below.)

● Genetic syndromes – Laryngomalacia may occur in association with genetic syndromes such
as Down syndrome or 22q11.2 deletion syndrome. (See "Down syndrome: Clinical features
and diagnosis" and "DiGeorge (22q11.2 deletion) syndrome: Clinical features and diagnosis".)

Patients with underlying genetic syndromes may have more severe symptoms because of
other syndromic features that cause breathing difficulties, cyanosis, and/or feeding problems
(eg, other airway abnormalities, neuromuscular disease, congenital heart disease) [1,20,21].

● Other associated airway abnormalities – Approximately 15 to 30 percent of infants with

laryngomalacia have additional airway anomalies such as subglottic stenosis, tracheomalacia,
vocal cord immobility, laryngeal clefts, or tongue base obstruction [2,9,22,23]. The presence
of additional airway abnormalities generally causes more severe airway obstruction [20].

● Prematurity – There is a higher prevalence of laryngomalacia and tracheomalacia among

infants born very preterm compared with term infants. In the available case series, preterm
infants accounted for approximately 15 percent of infants with isolated laryngomalacia and
up to 30 percent of those with combined laryngomalacia and tracheomalacia [2,3]. The risk of
airway abnormalities is greatest in preterm infants with significant neonatal respiratory
morbidity (eg, bronchopulmonary dysplasia and/or requiring intubation during the neonatal
intensive care unit hospitalization). (See "Complications and long-term pulmonary outcomes
of bronchopulmonary dysplasia", section on 'Central airway disease'.)

Preterm infants are also more likely to have feeding and swallowing difficulties. (See
"Neonatal oral feeding difficulties due to sucking and swallowing disorders", section on
 'Prematurity'.)

NATURAL HISTORY
In children who are otherwise healthy, laryngomalacia typically resolves over time as the child
grows. Symptoms typically peak at four to eight months of age and improve by 12 to 18
months; most patients outgrow stridor by 24 months of age [20]. In a review of three
retrospective studies including a total of 411 infants and children with laryngomalacia, 89
percent had resolution of symptoms within the first few years of life (time to resolution ranged
from 4 to 42 months) [24].

By contrast, laryngomalacia tends to persist in children who have underlying neuromuscular

disorders and genetic syndromes [1,25,26].

DIAGNOSIS
The diagnosis of laryngomalacia is suspected based upon the history and physical examination.
A presumptive diagnosis can be made based upon the characteristic features of inspiratory
"wet" stridor beginning in the newborn period and becoming more noticeable over the first few
months of life; worse in the supine position, improving when the infant is upright (see
'Presentation' above). The diagnosis is confirmed with awake flexible laryngoscopy ( movie 1
and movie 2).

Referral indications — Referral to a pediatric otolaryngologist is warranted for any infant or

child presenting recurrent or chronic stridor, especially if it has been present since birth or if the
child's symptoms are atypical for croup (eg, recurrent episodes of croup-like symptoms). (See
"Croup: Clinical features, evaluation, and diagnosis", section on 'Recurrent croup'.)

The otolaryngologist confirms the diagnosis with flexible fiberoptic laryngoscopy and guides
management. Although a presumptive diagnosis of laryngomalacia can often be made based
upon the history and physical examination alone, flexible fiberoptic laryngoscopy is generally
warranted to exclude other causes of recurrent/chronic stridor (eg, vocal cord paralysis or
dysfunction, laryngeal cleft, subglottic hemangiomas). (See 'Differential diagnosis' below.)

The urgency of referral is guided by symptom severity. Infants with severe symptoms warrant
expedited referral; those who have significant respiratory distress, apnea, desaturation, and/or
inability to feed generally warrant inpatient admission [20].
For infants with mild intermittent inspiratory stridor who are otherwise feeding and growing
well, nonurgent referral is appropriate.

Confirming the diagnosis — The definitive diagnosis of laryngomalacia is made with awake
flexible fiberoptic laryngoscopy [20]. Typical findings of laryngomalacia include an omega-
shaped epiglottis, collapse of the supra-arytenoid tissue, and short aryepiglottic folds
( movie 1 and picture 1). A retro-displaced epiglottis may also be present, especially in
children with underlying neurological disorders ( movie 2).

For children who have normal or equivocal findings on awake laryngoscopy yet have a clinical
presentation highly suggestive of laryngomalacia, drug-induced sleep endoscopy (DISE) may be
useful to evaluate for sleep variant laryngomalacia (also called state-dependent laryngomalacia)
[27]. Some children show signs of supraglottic collapse only during sleep. DISE can identify this
variant and help define the areas of supraglottic prolapse [28]. DISE is performed in the
operating room under anesthesia which permits evaluation of the airway in a sleep-like state.
We do not advise DISE in young infants. DISE is most commonly used to evaluate older children
with residual obstructive sleep apnea following adenotonsillectomy. The procedure is discussed
in greater detail separately. (See "Adenotonsillectomy for obstructive sleep apnea in children",
section on 'Drug-induced sleep endoscopy'.)

Additional evaluation — Once the diagnosis of laryngomalacia is confirmed, additional

evaluation may be warranted to evaluate for secondary airway lesions, swallowing
dysfunction/aspiration, sleep-disordered breathing, and/or gastroesophageal reflux disease
(GERD).

● Evaluation for secondary airway lesions – If there is clinical concern for a secondary airway
abnormality (eg, subglottic stenosis, tracheomalacia) we suggest ancillary airway evaluation
with airway radiographs (anteroposterior and lateral radiographs of the neck) and/or direct
laryngoscopy and bronchoscopy [20,22].

Secondary airway abnormalities may be suspected if:

• The infant has moderate to severe symptoms that are not commensurate with the findings
on fiberoptic laryngoscopy, or

• The infant's stridor is atypical for laryngomalacia (eg, expiratory or biphasic stridor or
associated with hoarseness)

Ancillary airway evaluation is lower yield in infants with mild symptoms that are typical of
laryngomalacia and consistent with the laryngoscopy findings; bronchoscopy is not routinely
 necessary in this setting [20].

● Swallow evaluation – A formal evaluation of swallowing function should be performed in

infants with feeding difficulties; choking, coughing, or regurgitating with feeds; and/or poor
weight gain [9,20,29]. The initial step is usually a clinical feeding evaluation by a speech-
language pathologist or occupational therapist, followed by a videofluoroscopic swallow
study (VFSS) and/or fiberoptic endoscopic evaluation of swallowing (FEES) if warranted based
upon the findings of the clinical evaluation. Additional details are provided separately. (See
"Neonatal oral feeding difficulties due to sucking and swallowing disorders", section on
'Diagnostic evaluation' and "Aspiration due to swallowing dysfunction in children", section on
'Evaluation'.)

The swallow evaluation provides an objective assessment of swallowing and airway protection
that informs management decisions regarding the need for feeding modifications or surgical
intervention. Approximately 15 percent of patients with moderate laryngomalacia and up to
70 percent with severe laryngomalacia demonstrate aspiration on formal swallow evaluation
[30].

● Polysomnography – A formal sleep study is not necessary in most infants with congenital
laryngomalacia. Technical challenges of performing polysomnography in young infants and
uncertainty regarding its diagnostic accuracy in this age group preclude using it as a routine
in this setting. Instead, we generally use the clinical criteria described below to characterize
the severity of airway obstruction, which informs management decisions. (See 'Severity
assessment' below.)

However, polysomnography can be useful in select circumstance (eg, if there is clinical

suspicion for central apnea, in older children with sleep-disordered breathing). Additional
details regarding polysomnography in infants and children are provided separately. (See
"Overview of polysomnography in infants and children" and "Evaluation of suspected
obstructive sleep apnea in children", section on 'Polysomnography'.)

● Diagnostic evaluation for GERD – Most infants and children with clinically significant
laryngomalacia are treated empirically with acid suppression therapy, and a diagnostic
evaluation for GERD is not necessary. (See 'Initial interventions (medical therapy)' below.)

However, a diagnostic evaluation for pathologic GERD may be appropriate in select cases (eg,
patients with severe or refractory symptoms). The diagnostic approach for GERD is described
elsewhere. (See "Gastroesophageal reflux disease in children and adolescents: Clinical
manifestations and diagnosis", section on 'Diagnostic approach'.)
Severity assessment — We use the Thompson classification system to characterize the severity
of laryngomalacia. It is based chiefly on the infant's symptoms [1,31]:

● Mild disease – In mild laryngomalacia, symptoms are generally limited to intermittent stridor.
Patients with mild laryngomalacia have normal oxygen levels (baseline resting oxygen
saturation >98 percent). They generally feed comfortably and have normal growth. They have
a coordinated suck-swallow-breath sequence, though they may occasionally cough, choke,
and/or regurgitate with feeding.

Approximately 40 percent of infants with laryngomalacia who present to a tertiary care

pediatric otolaryngology practice fall into the mild category [1].

● Moderate disease – Infants with moderate disease have persistent stridor at baseline. They
may have intermittent cyanosis, though their resting oxygen saturation levels are generally in
the normal range (approximately 95 percent). They usually have associated feeding difficulty
caused by difficulty coordinating the suck-swallow-breath sequence. These patients tend to
tire during feeding and are described by caregivers as difficult to feed. They also have
frequent coughing and choking episodes, regurgitation, and post-prandial emesis. Without
intervention, these problems can lead to aspiration or weight loss secondary to caloric
expenditure from increased work of breathing.

Approximately 40 percent of infants with laryngomalacia who present to a tertiary care

pediatric otolaryngology practice fall into the moderate category [1].

● Severe disease – Infants with severe disease have persistent stridor at baseline that is
associated with recurrent cyanosis, apneic pauses, feeding difficulties, aspiration, and growth
failure. They have pronounced suprasternal and subcostal retractions that can lead to pectus
excavatum ( movie 3). They generally have low resting oxygen saturation levels
(approximately 85 to 90 percent). Without intervention, chronic hypoxemia can lead to
pulmonary hypertension and cor pulmonale. As discussed below, patients with severe disease
often require surgical intervention. (See 'Severe laryngomalacia' below.)

Approximately 20 percent of infants with laryngomalacia who present to a tertiary care

pediatric otolaryngology practice fall into the severe category [1].

Various other severity classification schemas for laryngomalacia have been described. Some are
based purely on anatomic features without correlation to symptom burden [32], while others
have attempted to account for both symptoms and anatomic findings [33,34].
DIFFERENTIAL DIAGNOSIS
The differential diagnosis includes other causes of recurrent stridor that present in infancy,
including subglottic stenosis, vocal cord paralysis, vascular rings, laryngeal clefts, subglottic
hemangiomas, tracheomalacia, and recurrent croup ( figure 3 and table 1A-B).
Laryngomalacia is distinguished from these based upon the endoscopic examination. The
assessment of stridor in children is discussed separately. (See "Assessment of stridor in
children".)

MANAGEMENT
The management of laryngomalacia depends upon the severity, as discussed in the following
sections ( algorithm 1). Our suggested approach is generally consistent with the
recommendations of the International Pediatric Otolaryngology Group (IPOG) [20].

The symptoms of laryngomalacia are burdensome and can create fear and anxiety in the
parents/caregivers with substantial negative impact on quality of life for both the infant and the
parents/caregivers [35-37]. While, in most cases, this is a self-limited condition that resolves
over time and can be managed expectantly, it is important to observe and monitor for symptom
progression and adjust management accordingly. Surgical intervention is reserved for a small
subset of patients with severe symptoms that persist despite medical management.

Mild laryngomalacia — Infants with mild laryngomalacia (intermittent mild stridor with normal
growth and no other symptoms), we suggest conservative management with supportive care
and observation [20,38]. Stridor usually resolves by 12 to 18 months of age in these infants. (See
'Natural history' above.)

Conservative management includes the following:

● Ongoing monitoring to ensure that weight gain is adequate. (See "Normal growth patterns in
infants and prepubertal children".)

● Anticipatory guidance for the parents/caregivers regarding the typical course of

laryngomalacia (ie, that it usually resolves as the infant grows). (See 'Natural history' above.)

● For infants with frequent regurgitation or other concerns for gastroesophageal reflux (GER),
simple measures that may be helpful include a trial of thickened feeds, upright positioning
after feeds, and avoiding overfeeding [18]. If there is no improvement with these measures, a
 trial of acid suppression therapy is reasonable. (See "Gastroesophageal reflux in infants",
section on 'Additional options for infants with GERD or problematic reflux'.)

Patients should have initial follow-up for symptom assessment within a month. If the patient is
stable or improving, subsequent follow-up visits can be spaced to every three to six months
[20].

Moderate laryngomalacia — Infants and children with moderate laryngomalacia (persistent

stridor associated with feeding difficulty and poor weight gain) should be managed in
collaboration with a pediatric otolaryngologist and a clinician experienced in infant swallowing
and feeding disorders (eg, a speech or occupational therapist) [20]. Involvement of other
specialists may be appropriate depending on the clinical circumstances (eg, a dietitian for
infants with poor weight gain, a gastroenterologist for patients with severe GER, a neurologist if
there is concern for undiagnosed neuromuscular disease).

Medical management may be sufficient for some infants with moderate laryngomalacia [39];
however, infants with persistent or progressive symptoms despite medical management may
require surgical intervention.

Initial interventions (medical therapy) — For most patients with moderate laryngomalacia,
we suggest initial medical therapy rather than proceeding directly to surgical intervention.

Medical management includes [20,39]:

● Acid suppression therapy – Acid suppression therapy consists of a histamine type 2

receptor antagonist (H2RA) or proton pump inhibitor (PPI). The choice between an H2RA or
PPI is based on cost, availability, and preferences of the clinician and patient. There is no
evidence to suggest that one agent is more effective than the other in this setting or that
there is additional benefit from using both medications. The dosing, administration, and
side effects of these medications are summarized in the table ( table 2) and discussed in
detail separately. (See "Gastroesophageal reflux disease in children and adolescents:
Management", section on 'Pharmacotherapy'.)

Data supporting H2RAs and PPIs in patients with laryngomalacia are limited to
observational studies with variable findings [17,18,40]. In a retrospective study of 199
infants with isolated laryngomalacia (ie, not associated with genetic or neuromuscular
disorders) who were started on acid suppression therapy (largely with H2RAs) by age six
months and followed for up to one year, the proportion of children with airway symptoms
declined from 97 to 40 percent and the proportion of children with dysphagia symptoms
declined from 75 to 40 percent [17]. However, given the lack of control group in this study, it
 is unclear if the observed symptom improvements were due to acid suppression therapy or
if this merely reflects the expected natural history of laryngomalacia. (See 'Natural history'
above.)

By contrast, another retrospective study did not detect any improvements in respiratory
exacerbations or need for surgery associated with use of acid suppressive therapy. In this
study, which included 236 infants and children with laryngomalacia, 55 percent were
treated with acid suppression therapy (consisting of H2RAs in 50 percent, PPIs in 20
percent, and H2RA plus PPI in 30 percent) [18]. In this cohort, acid suppression therapy was
associated with a nearly two-fold increased rate of hospitalization for respiratory symptoms
and more than three-fold higher likelihood of requiring supraglottoplasty. Given the
retrospective nature of the data, confounding may explain the findings (ie, more severely
affected patients are more likely to be treated with acid suppression therapy, and this may
explain the higher rates of hospitalization and surgery in this group).

● Feeding modification – Swallowing problems are common in infants with moderate to

severe laryngomalacia [29]. Improving feeding is essential for the quality of life for
caregivers and infants.

Feeding interventions should be tailored to the individual patient and may include
measures such as texture modification (eg, thickened feeds), paced feedings, or use of
various special nipples for bottle feeding to reduce flow and minimize aerophagia. These
interventions are discussed in greater detail separately. (See "Neonatal oral feeding
difficulties due to sucking and swallowing disorders", section on 'Management approach'
and "Gastroesophageal reflux in infants", section on 'Additional options for infants with
GERD or problematic reflux'.)

In a study of 236 infants and children with laryngomalacia who were managed at a single
tertiary center, thickening feeds was associated with a lower risk of hospitalization for
respiratory complications [18].

● High-calorie feeds to promote weight gain – The approach to nutritional support for
infants with poor weight gain is discussed in detail separately. (See "Poor weight gain in
children younger than two years in resource-abundant settings: Management", section on
'Nutritional therapy'.)

Persistent or progressive symptoms despite medical therapy — In most infants and

children with moderate laryngomalacia, symptoms stabilize and improve with medical
management. However, approximately 20 to 30 percent progress to severe disease, requiring
surgical intervention, nasogastric (NG) or gastronomy (G) tube feeds, or artificial airway
 support [1,38]. Those with comorbid conditions and synchronous airway lesions are more
likely to progress to severe disease.

For most patients who develop progressively worsening symptoms despite medical
management, we suggest supraglottoplasty, as discussed below. (See 'Supraglottoplasty'
below.)

Severe laryngomalacia — For infants and children with severe laryngomalacia (persistent
stridor associated with severe retractions, cyanosis, apneic episodes, severe feeding difficulties,
aspiration, and/or growth failure), initial management consists of the same medical therapies
that are used for moderate disease (ie, gastric acid suppression therapy and feeding
modifications, including NG or G tube feedings if the infant is unable to feed orally). (See 'Initial
interventions (medical therapy)' above.).

However, in severely affected patients, symptoms often do not improve with medical therapy
alone, and most patients in this category require surgical intervention.

The urgency of surgical intervention depends on the clinical circumstances. In patients with
more extreme manifestations (eg, severe recurrent apneic and cyanotic spells), surgical
intervention should be expedited simultaneously with implementing medical therapies. In less
extreme cases, it is usually feasible to provide an initial trial of medical therapy before
proceeding to surgery.

Supraglottoplasty — Supraglottoplasty is the procedure of choice for treatment of severe or

persistent laryngomalacia. Supraglottoplasty removes redundant supraglottic tissue thereby
reducing the severity of airway obstruction ( picture 2 and movie 4).

● Indications for surgery – Surgical intervention is appropriate for patients with severe
symptoms despite medical therapy. Indications for surgery include any of the following [20]

• Apnea (sleep or awake)

• Persistent cyanosis
• Respiratory distress
• Pectus excavatum
• Growth failure due to feeding difficulty
• Cor pulmonale and pulmonary hypertension

There is considerable institutional variability in the use of supraglottoplasty for

management of laryngomalacia, with some specialized centers performing only a handful
of procedures annually, and other centers reporting >200 supraglottoplasties per year
 [41,42]. As experience with the procedure has grown and given the low complication rate of
the procedure, some pediatric otolaryngologists offer supraglottoplasty as a treatment
option for patients with moderate disease who have substantially impaired quality of life.
Several studies have demonstrated improvements in quality of life following surgical
intervention that correlate with parental/caregiver goals of reducing time spent feeding the
infant, achieving successful breastfeeding, and securing child care placement thereby
reducing time away from work [35-37]. However, high levels of parental satisfaction with
surgery should be balanced against the risks and expense of supraglottoplasty for what is a
self-limited disease in most children. In our practice, we generally reserve supraglottoplasty
for severely affected patients.

● Supraglottoplasty procedure – Supraglottoplasty is performed under general anesthesia

by operating through an endoscope in the oral cavity. The aryepiglottic folds are divided,
and the redundant supra-arytenoid tissue that collapses in the airway is removed
( picture 2 and movie 4). The result is a wider opening in the supraglottic airway.

Supraglottoplasty may be combined with surgery to address multilevel airway obstruction

in children with tracheal disease, tongue base disease, or syndromes associated with
anatomic airway obstruction such as Pierre Robin sequence [43]. Success rates are lower in
these high-risk patients, and if supraglottoplasty is unsuccessful, tracheostomy placement
may ultimately be required. (See 'Failure of supraglottoplasty' below.)

● Recovery and follow-up – Most patients are observed in the hospital and can be
discharged the day after surgery [44]. Patients with underlying medical comorbidities,
syndromes, and synchronous airway lesions may require observation in the pediatric
intensive care unit (PICU) setting; some may require short-term intubation [45,46]. In
addition, PICU admission is appropriate for patients who experience significant
perioperative airway obstruction or desaturation and for young infants (<2 months),
especially preterm infants, given the potential for postoperative apnea in these patients.
However, low-risk patients who are otherwise healthy generally do not require PICU
admission following supraglottoplasty [47,48]. There are few data on the safety of
outpatient supraglottoplasty. In a study reporting on 975 infants and children who
underwent supraglottoplasty at a single center over a 10-year period, 24 percent were
discharged the same day, 63 percent were observed overnight, and 13 percent required ≥2
nights in the hospital [44]. Factors associated with longer length of stay included young age
(ie <5 months); history of apnea; growth failure or G-tube dependence; previous admission
for airway problems; and underlying diagnosis of cerebral palsy, genetic syndrome, or
 cardiac anomaly. Among patients who were discharged the same day or observed
overnight, 2.5 percent had an unplanned readmission within 30 days after discharge.

Follow-up after surgery typically occurs at two to three weeks.

The optimal duration of acid suppression therapy after surgery is uncertain. Most
otolaryngologists continue acid suppression therapy at least until the surgical site has
healed. Some clinicians continue acid suppression until there are no further feeding or
aspiration problems.

● Efficacy – In experienced hands, supraglottoplasty can produce dramatic improvements in

breathing, feeding, and growth with little morbidity [49,50]. Opening the airway improves
the suck-swallow-breath sequence. In patients with aspiration and without underlying
neurological disease, aspiration often resolves after surgical intervention.

Reported success rates for supraglottoplasty range from 60 to 95 percent [51,52]. The
definition of success varies from study to study; it generally refers to improvement in
respiratory status and feeding problems without the need for additional surgical
intervention. Success rates tend to be lower in children with concomitant neurologic
disease or genetic syndromes. These patients more frequently require revision surgery,
tracheostomy, or feeding tube insertion [51]. (See 'Failure of supraglottoplasty' below.)

Airway obstruction symptoms (eg, stridor, cyanotic/apneic episodes) usually improve

dramatically after surgery. However, patients with preoperative obstructive sleep apnea
(OSA) may continue to have persistent OSA despite intervention. In a meta-analysis of four
observational studies involving children with sleep-disordered breathing due to
laryngomalacia, supraglottoplasty was associated with improvements in the apnea-
hypopnea index (AHI) and oxygen saturation [53]. Two other meta-analyses reported
similar findings [2,54]. Patients with a preoperative AHI >12 demonstrate greater
improvement; those younger than seven months of age at time of surgery also
demonstrate greater impact on AHI [53]. In infants with neurologic disease, other
congenital anomalies, or genetic syndromes, OSA tends to persist longer and can take up
to four to five years to resolve [55]

Swallowing function improves gradually after supraglottoplasty [41,56]; the pace of

improvement varies, depending on whether the infant has other comorbidities. In infants
without underlying neurological disease, genetic syndromes, prematurity, or coexisting
unrepaired airway lesions, swallowing function and aspiration gradually improve over
several months to a year following surgery [29,57]. In one study that included 143
nonsyndromic patients who underwent supraglottoplasty, 25 percent had resolution of
 dysphagia by 4 months after surgery, 50 percent by 10 months, and 75 percent by 14
months [57]. Persistent feeding difficulties after supraglottoplasty are more common in
preterm infants [58]. Patients who do not have sufficient improvement in feeding may
require NG or G tube placement for nutrition. Some may require revision surgery. (See
'Failure of supraglottoplasty' below.)

Several studies have documented good catch-up growth following supraglottoplasty

among infants with poor weight gain preoperatively [49,59].

● Complications – Possible complications of supraglottoplasty include supraglottic or glottic

scarring, chronic aspiration, and dysphonia. These are uncommon, occurring in <10 percent
of cases [51]. Some patients may require revision surgery if abnormal scarring occurs. (See
'Failure of supraglottoplasty' below.)

The risks and benefits of supraglottoplasty should be carefully considered in children with
underlying neuromuscular disease. Neuromuscular disease is not a contraindication to
supraglottoplasty, but the benefit of improving airway obstruction must be weighed
against the risk of worsening aspiration in this setting [20].

Failure of supraglottoplasty — Revision surgery may be required for those who do not
improve after surgery. Revision surgery may also be required if too little tissue is removed at
the initial operation, or abnormal scarring occurs. Revision surgery rates are higher in those
with severe GER, neuromuscular disease, hypotonia, or underlying genetic syndromes
[25,26,60-62].

If revision surgery is required, further investigation may be warranted to identify potential

underlying contributing factors (eg, pathologic or undertreated GER, undiagnosed neurologic
conditions such as a Chiari malformation).

Tracheostomy to bypass the supraglottic airway is usually reserved for high-risk patients with
supraglottoplasty failure (ie, those with multilevel airway obstruction involving the trachea or
tongue base, or syndromes associated with anatomic airway obstruction such as Pierre Robin
sequence). Tracheostomy is rarely employed as a first-line operation for laryngomalacia.

Alternatives to surgery — For patients with unacceptably high surgical risk or if the
parents/caregivers wish to avoid surgery, the main alternatives to surgery are noninvasive
ventilatory support modalities such as continuous positive airway pressure (CPAP; which can
be used in the home setting), or high-flow nasal cannula (HFNC; which is generally limited to
inpatient care settings). These modalities have been used in children with laryngomalacia
with variable success and compliance [63]. The positive pressure provided by CPAP or HFNC
 may reduce airway obstruction and improve respiratory symptoms in children with moderate
to severe laryngomalacia. However, it increases the risk of feeding difficulties and aspiration.
Thus, for children with laryngomalacia who are managed with these modalities, oral feeding
is often deemed unsafe, and NG or G tube feeds are required.

The use of CPAP in the management of pediatric OSA is discussed in greater detail separately.
(See "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea".)

OUTCOME
The prognosis for infants and children with laryngomalacia depends on the severity and
whether there are associated comorbidities.

● Mild to moderate disease without underlying medical conditions – In children who are
otherwise healthy, laryngomalacia usually resolves over time as the child grows. (See 'Natural
history' above.)

● Severe disease – Most patients with severe laryngomalacia require surgery, as discussed
above (see 'Severe laryngomalacia' above). There are few data on long-term outcomes
following supraglottoplasty [51,64]. In the authors' experience, most patients treated with
supraglottoplasty do well in the long-term. In our experience, approximately 85 percent of
surgically treated patients recover well and do not require any further airway interventions.
Approximately 5 percent of patients require revision surgery (eg, dividing a surgical site scar,
removing additional redundant supra-arytenoid tissue, or suspending the epiglottis), which
usually successfully addresses any residual symptoms. However, approximately 10 percent of
patients do not achieve adequate improvement in breathing and swallowing function after
supraglottoplasty. These patients usually require a combination of other interventions,
including noninvasive positive airway pressure, enteral feeding via a nasogastric or
gastrostomy tube, and/or other airway surgery (eg, tongue base procedure or tracheostomy).

● Patients with underlying neuromuscular or genetic conditions – Laryngomalacia tends to

persist in these patients. Supraglottoplasty may improve symptoms, but many patients
continue to have at least moderate symptoms following surgery [1,25,26]. Approximately 30
to 50 percent of patients require revision surgery and 10 to 40 percent ultimately require
tracheostomy [25,26].

SUMMARY AND RECOMMENDATIONS

● Epidemiology – Congenital laryngomalacia is the most common cause of chronic or recurrent
stridor in infancy. The reported prevalence is approximately three to four cases per 10,000 live
births. (See 'Epidemiology' above.)

● Anatomy and pathogenesis – Congenital laryngomalacia is characterized by short

aryepiglottic folds, an omega-shaped epiglottis, and collapse of the supra-arytenoid tissue
into the glottic inlet during inspiration ( picture 1 and movie 1). The pathogenesis of
laryngomalacia is not fully understood. It likely results from a combination of neurologic,
anatomic, and inflammatory abnormalities leading to diminished tone of the supraglottic
tissue and supporting musculature. (See 'Anatomy' above and 'Pathogenesis' above.)

● Clinical features

• Presentation – Infants with congenital laryngomalacia usually present with inspiratory

stridor that begins in the newborn period and peaks at four to eight months of age. Stridor
worsens with activities such as crying, agitation, excitement, feeding, or supine positioning.
The severity can range from mild intermittent symptoms to severe airway obstruction
associated with respiratory distress (eg, retractions ( movie 3), tachypnea), apnea, and
cyanotic episodes. Feeding difficulties are common and can range from mild (occasional
coughing and regurgitation during feeding) to severe (recurrent aspiration events or
growth failure dure to inability to feed). (See 'Presentation' above and 'Severity assessment'
above.)

• Associated conditions – Comorbid medical conditions are common in infants and children
with congenital laryngomalacia and may include (see 'Associated conditions' above):

- Gastroesophageal reflux (GER)

- Neuromuscular disorders
- Genetic syndromes (eg, Down syndrome or 22q11.2 deletion syndrome)
- Secondary airway abnormalities (eg, subglottic stenosis, tracheomalacia)
- Prematurity

● Natural history – In children who are otherwise healthy, laryngomalacia typically resolves
over time as the child grows. Most patients outgrow stridor by 24 months of age. By contrast,
laryngomalacia tends to persist in children who have underlying neuromuscular disorders
and genetic syndromes. (See 'Natural history' above and 'Outcome' above.)

● Referral indications – Referral to a pediatric otolaryngologist is warranted for any infant or

child presenting recurrent or chronic stridor. The urgency of referral is guided by symptom
severity. Infants with severe symptoms warrant expedited referral; those who have significant
 respiratory distress, apnea, desaturation, and/or inability to feed generally warrant inpatient
admission. For infants with mild intermittent inspiratory stridor who are otherwise feeding
and growing well, nonurgent referral is appropriate. (See 'Referral indications' above.)

● Diagnosis – The diagnosis of laryngomalacia is made with awake flexible fiberoptic

laryngoscopy demonstrating an omega-shaped epiglottis, short aryepiglottic folds, and
collapse of the supra-arytenoid tissue into the glottic inlet during inspiration ( movie 1 and
picture 1). A retro-displaced epiglottis may also be present ( movie 2), especially in
children with underlying neurological disorders. (See 'Confirming the diagnosis' above.)

Once the diagnosis of laryngomalacia is confirmed, additional evaluation may be warranted

in some cases to evaluate for secondary airway lesions, swallowing dysfunction/aspiration,
sleep-disordered breathing, and/or gastroesophageal reflux disease (GERD). (See 'Additional
evaluation' above.)

● Differential diagnosis – The differential diagnosis includes other causes of recurrent stridor
presenting in infancy, including subglottic stenosis, vocal cord paralysis, vascular rings,
laryngeal clefts, subglottic hemangiomas, tracheomalacia, and recurrent croup ( figure 3
and table 1A-B). Laryngomalacia is distinguished from these based upon the endoscopic
examination. (See "Assessment of stridor in children".)

● Management of mild disease – For infants and children with mild laryngomalacia (ie, those
with intermittent stridor but who otherwise feed comfortably and have normal growth), we
suggest conservative management with supportive care and observation (Grade 2C). These
patients should have ongoing monitoring to ensure weight gain is adequate ( algorithm 1).
(See 'Mild laryngomalacia' above.)

● Management of moderate to severe disease – Infants and children with moderate to severe
laryngomalacia (persistent stridor associated with feeding difficulty, poor weight gain,
retractions, apnea, and/or cyanosis) should be managed in collaboration with a pediatric
otolaryngologist and a clinician experienced in infant swallowing and feeding disorders (eg, a
speech or occupational therapist). Our suggested approach to management is as follows
( algorithm 1) (see 'Management' above):

• Initial interventions – For most patients with moderate or severe laryngomalacia, we

suggest initial medical therapy rather than proceeding directly to surgical intervention
(Grade 2C). Medical management includes (see 'Initial interventions (medical therapy)'
above):
 - Acid suppression therapy – For all patients with moderate or severe laryngomalacia, we
suggest empiric therapy with an acid suppression agent (eg, a histamine type 2 receptor
antagonist [H2RA] or proton pump inhibitor [PPI]) (Grade 2C). Dosing, administration,
and side effects of these medications are summarized in the table ( table 2) and
discussed in detail separately. (See "Gastroesophageal reflux disease in children and
adolescents: Management", section on 'Pharmacotherapy'.)

- Feeding modification – Feeding interventions should be tailored to the individual patient

and may include measures such as texture modification (eg, thickened feeds), paced
feedings, or use of various special nipples for bottle feeding to reduce flow and minimize
aerophagia. Infants with poor weight gain may require high-calorie formula or breast
milk supplements to promote weight gain. These interventions are discussed in greater
detail separately. (See "Neonatal oral feeding difficulties due to sucking and swallowing
disorders", section on 'Management approach' and "Gastroesophageal reflux in infants",
section on 'Additional options for infants with GERD or problematic reflux' and "Poor
weight gain in children younger than two years in resource-abundant settings:
Management", section on 'Nutritional therapy'.)

• Persistent severe symptoms – For patients with severe laryngomalacia that persists
despite medical management, we suggest supraglottoplasty (Grade 2C). Supraglottoplasty
removes redundant supraglottic tissue thereby reducing the severity of airway obstruction
( picture 2). Complications are uncommon (<10 percent) and may include supraglottic or
glottic scarring, chronic aspiration, and dysphonia. Revision surgery may be required in
some patients, particularly those with underlying neuromuscular disease or genetic
syndromes. (See 'Supraglottoplasty' above.)

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Topic 135070 Version 5.0
GRAPHICS

Congenital laryngomalacia
Images obtained during flexible fiberoptic laryngoscopy in an infant with congenital laryngomalacia:
(Image A) During exhalation, note the omega-shaped epiglottis (thick arrow) and redundant supra-
arytenoid tissue (arrows).
 (Image B) During inspiration, note collapse of the epiglottis (thick arrow) and redundant supra-
arytenoid tissue (arrows) into the glottic inlet.

Graphic 79457 Version 3.0

Intrinsic laryngeal musculature with relative positions of the thyroid, cricoid,
and arytenoid cartilages

Reproduced with permission from Garrett CG, Ossoff RH. Hoarseness. Med Clin N Am 1999; 83:115. Copyright 1999 W.B. Saunders
Company.

Graphic 56206 Version 2.0

Anatomic classification of congenital laryngomalacia

This figure summarizes the Olney classification schema of congenital laryngomalacia. In infants and
children with congenital laryngomalacia, supraglottic tissue collapses into the glottic inlet during
inspiration. The Olney classification categorizes laryngomalacia into three types based on supraglottic
morphology as outlined above.

Graphic 147056 Version 1.0

Causes of stridor in children by location

* Acute or subacute onset.

Graphic 101485 Version 2.0

Congenital anomalies associated with stridor

Malformation Characteristics
Nose* Nasal deformities Choanal atresia or agenesis, septum deformities, turbinate
hypertrophy, vestibular atresia, or stenosis.
Pharynx* Craniofacial Anomalies causing facial retrusion are associated with upper
anomalies airway obstruction, including Crouzon, Pierre Robin, and Apert
syndromes.
Tongue Macroglossia and glossoptosis.
Larynx Laryngomalacia Most common cause of chronic stridor in infants. Almost all
patients present by 6 weeks of age. Symptoms are more
pronounced after upper respiratory infections.
Laryngeal webs 75% located in the glottic area. Complete webs cause
respiratory distress at birth and partial webs produce stridor,
weak cry, and different degrees of respiratory distress.
Associated anomalies are common.
Laryngeal cysts If located in supraglottic area, may cause respiratory distress
and stridor.
Laryngeal clefts Characterized by abnormal communication between the larynx
and pharynx, sometimes extending downward between the
trachea and esophagus. Patients may present with aspiration,
cough, swallowing difficulties, respiratory distress, hoarse cry,
or occasionally with stridor; often associated with other
congenital anomalies.
Subglottic Presents as with stridor and respiratory distress, usually
hemangioma worsening during the first few months of life. Often associated
with cutaneous hemangiomas.
Subglottic stenosis May be congenital but more often acquired secondary to
intubation. Usually located 2 to 3 mm below the glottis.
Vocal cord Idiopathic or secondary to a neurologic disorder (including
paralysis Chiari II malformation, hydrocephalus, meningomyelocele,
hypoxic cerebral palsy, and cerebral hemorrhage) [1,2] .
Trachea ¶ Tracheal stenosis Usually presents with stridor or both stridor and wheezing. If
stenosis is significant, respiratory distress occurs.
Vascular rings or 74% of vascular rings are symptomatic. The airway
slings compression usually is intrathoracic, causing expiratory stridor
Associated anomalies are common.
Tracheomalacia Often associated with other congenital anomalies. May be
secondary to a vascular ring or cysts. Worsens with upper
 respiratory infections, crying, coughing, or feeding. May cause
severe spells with cyanosis.
Bronchi and Bronchogenic cyst May occur at any point throughout the tracheobronchial tree.
distal airways ¶ Typically present during childhood with recurrent coughing,
wheezing, or pneumonia, but may become symptomatic
during infancy or adulthood or present as an incidental finding
on chest radiographs.

* Noise generated from the nose or pharynx is typically low in pitch and is referred to as snoring or
stertor.
¶ Noise generated from the trachea, bronchi, or distal airways is mostly wheezing.

References:
1. Nisa L, Holtz F, Sandu K. Paralyzed neonatal larynx in adduction. Case series, systematic review and analysis. Int J Pediatr
Otorhinolaryngol 2013; 77:13.
2. Holinger LD, Holinger PC, Holinger PH. Etiology of bilateral abductor vocal cord paralysis: a review of 389 cases. Ann Otol
Rhinol Laryngol 1976; 85:428.

Graphic 62718 Version 8.0

Noncongenital causes of stridor in children

Typical age of presentation

Infants
and Preschool Inspiratory
Cause School-
Neonate toddlers (3 to 5 Adolescents stridor
aged
(6 to 24 years)
months)
Acute or subacute onset
Viral croup X X +
(laryngotracheitis) ¶

Spasmodic croup X X +

Bacterial X X X +
tracheitis ¶

Epiglottitis X X X +
Retropharyngeal X X +/–
abscess

Peritonsillar X X X +/–
abscess

Inducible laryngeal X X +
obstruction (vocal
cord dysfunction or
paradoxical vocal
cord motion)

Foreign body X X +
aspiration Δ
 Anaphylaxis X X X X +

Airway burn X X X X +

Postextubation X X X X +

Therapeutic X X
hypothermia

Chronic
Congenital X X +/–
anomalies

Vocal cord X X X X X +
paralysis ¶
Subglottic stenosis X X X X X +

Tumor X X X X X +/–

Recurrent X X +
respiratory
papillomatosis
 Hypocalcemic X X +/–
laryngeal spasm

+: usually present; +/–: may or may not be present; PICU: pediatric intensive care unit; URI: upper
respiratory tract infection.
* Any obstructive process that leads to a fixed airway narrowing will produce both inspiratory and
expiratory noise.
¶ Onset either acute or subacute/gradual.
Δ Foreign body aspiration can occur in any age group but is most common in toddlers and preschool-
aged children.

Graphic 101526 Version 8.0

Overview of management of congenital laryngomalacia

This figure summarizes our suggested approach to managing infants with congenital laryngomalacia. A
presumptive diagnosis of laryngomalacia can often be made based upon the history and physical
examination alone. However, any infant or child presenting recurrent or chronic stridor should be
referred to a pediatric otolaryngologist for endoscopic evaluation to exclude other causes. Refer to
UpToDate's topic on congenital laryngomalacia for additional details, including a discussion of the
evidence supporting our approach.
GERD: gastroesophageal reflux disease; H2RA: histamine type 2 receptor antagonist; PPI: proton pump
inhibitor; SpO2: peripheral oxygen saturation.
* The urgency of referral is guided by symptom severity. Infants with severe symptoms warrant
expedited referral; those who have significant respiratory distress, apnea, desaturation, and/or inability
to feed generally warrant inpatient admission. For infants with mild intermittent inspiratory stridor who
are otherwise feeding and growing well, nonurgent referral is appropriate.
¶ In infants with mild laryngomalacia, symptoms usually resolve by 12 to 18 months of age. These
patients are managed conservatively with supportive care and observation. The initial follow-up visit
should occur within a month. If the patient is stable or improving, subsequent follow-up visits can be
spaced to every 3 to 6 months Parents/caregivers should receive anticipatory guidance regarding the
typical course and instructions on when to seek care. Feeding modification is not necessary for all infants
with mild laryngomalacia but may be warranted if there is frequent regurgitation. Simple measures that
may be helpful include a trial of thickened feeds, upright positioning after feeds, and avoidance of
overfeeding. Refer to UpToDate's topics on swallowing dysfunction and gastroesophageal reflux in infant
for additional details.
Δ Medical therapy for moderate or severe laryngomalacia includes both:
Acid suppression therapy with either an H2RA or PPI. The choice between an H2RA or PPI is based
upon cost, availability, and preferences of the clinician and caregivers. There is no evidence to
suggest that one agent is more effective or that there is additional benefit from using both
medications.
Feeding modification(s) should be tailored to the individual patient and may include measures
such as texture modification (eg, thickened feeds), paced feedings, or use of various special
nipples for bottle feeding to reduce flow and minimize aerophagia. Infants with poor weight gain
may require high-calorie formula or breast milk supplements to promote weight gain.
◊ Supraglottoplasty is the procedure of choice for treatment of severe or persistent laryngomalacia.
Supraglottoplasty removes redundant supraglottic tissue thereby reducing the severity of airway
obstruction. The urgency of surgical intervention depends on the clinical circumstances. In patients with
more extreme manifestations (eg, severe recurrent apneic and cyanotic spells), surgical intervention
should be expedited simultaneously with implementing medical therapies. In less extreme cases, it is
usually feasible to provide an initial trial of medical therapy before proceeding to surgery.

Graphic 147705 Version 1.0

Drugs demonstrated to be effective for gastroesophageal reflux disease in
children

Type of Recommended oral Adverse Useful dose forms

medication dose effects/precautions * for children ¶
Proton pump inhibitors (PPIs) Δ◊
Omeprazole Infants 1 to 11 months Safety data for long- Capsules can be
(daily): term use of PPIs in opened and sprinkled
3 to <5 kg – 2.5 mg children are in general on soft food (10, 20,
5 to <10 kg – 5 mg reassuring * . and 40 mg)
≥ 10 kg – 10 mg Frequent (2 to 14%) – Flavored oral
Headache, diarrhea, suspension (2 mg/mL
Children ≥1 year:
abdominal pain, Granules for oral
1 mg/kg daily, given nausea, rash, suspension (2.5 and
30 minutes before constipation. 10 mg)
meal(s) §
Infrequent or rare –
May increase to 1 Increased risk of C.
mg/kg twice daily if difficile and other
needed for enteric infections;
symptomatic increased risk for lower
improvement respiratory tract
Adults: infections in infants
20 or 40 mg once (pediatric reports).
daily Malabsorption of
magnesium, calcium,
and, to a lesser extent,
vitamin B12 and iron
(adult reports).
United States FDA
approval is for use in
pediatric patients 1
month and older.
Omeprazole Similar to omeprazole Similar to other PPIs * . Capsules should not
and sodium Avoid using in patients be opened (20 and 40
bicarbonate on sodium-restricted mg capsules)
diets; contains 303 mg Powder for oral
(13 mmol) sodium per suspension should be
20 or 40 mg capsule; dissolved in water
460 mg (20 mmol) only (20 or 40 mg
sodium per 20 or 40 mg packets)
packet.
 United States FDA
approval is for adults 18
years and older.
Esomeprazole Infants 1 to 11 months Similar to other PPIs * . Capsules can be
(daily): Indication in infants is opened and sprinkled
3 to 5 kg – 2.5 mg for erosive esophagitis on soft food (20 and
5 to 7.5 kg – 5 mg due to acid-mediated 40 mg)
7.5 to 12 kg – 10 mg GERD. Granules for oral
suspension (2.5, 5, 10
Children 1 to 11 years
20, and 40 mg packet
(daily, given 30 minutes
before first meal each Intravenous
day): formulation
available ¥
Weight <20 kg – 10
mg
Weight >20 kg – 10
mg or 20 mg §
Children ≥12 years and
adults:
20 or 40 mg daily

Lansoprazole Infants and children: Similar to other PPIs * . Capsules can be

1 mg/kg daily, given opened and sprinkled
30 minutes before on soft food, or given
meal(s) § via NG or other
May increase to 1 enteral tube
mg/kg twice daily, if suspended in apple
needed, for juice (15 and 30 mg
symptomatic capsules)
improvement Flavored oral
Adults: suspension (3 mg/mL
15 to 30 mg once Orally disintegrating
daily tablets can be
dissolved in the
mouth or suspended
in water and given by
oral syringe or NG or
other enteral tube (15
and 30 mg tablets)
Dexlansoprazole Children ≥12 years and Similar to other PPIs * . Capsules can be
adults: opened and sprinkled
30 mg once daily on applesauce and
consumed
immediately or
 suspended in water
and given by oral
syringe (30 mg
capsules)
Orally disintegrating
tablets can be
dissolved in the
mouth or suspended
in water and given by
oral syringe or NG or
other enteral tube (30
mg tablets)
Pantoprazole Children ≥5 years: Similar to other PPIs * . Oral tablets should be
Weight 15 to <40 kg swallowed whole (20
– 20 mg and 40 mg).
Weight ≥40 kg – 40 Granules for oral
mg suspension (40 mg
Adults: packets)
40 mg once daily Intravenous
formulation
available ¥
Rabeprazole Children ≥12 years and Similar to other PPIs * . Oral tablets should be
adults: swallowed whole (20
20 mg once daily, mg)
given 30 minutes
before the first meal
each day

Histamine2 receptor antagonists (H2RAs) Δ‡†

Cimetidine Children: Safety data for the use Oral tablets may be
30 to 40 mg/kg per of H2RAs in children are crushed (200, 300,
day divided in 4 in general reassuring. 400, and 800 mg)
doses § H2RAs produce less Flavored oral solution
Adult dose: profound acid (300 mg/5 mL)
suppression than PPIs, Intravenous
400 to 800 mg twice
which may be an formulation
daily
advantage in some available ¥
clinical scenarios * .
Tachyphylaxis
(tolerance) commonly
develops with chronic
use (ie, >6 weeks).
Frequent – Headache,
dizziness, diarrhea,
 abdominal pain,
somnolence (adult
reports).
Infrequent or rare –
CNS disturbance,
gynecomastia,
idiosyncratic or
immune-mediated
hypersensitivity
including organ toxicity
(liver, kidney) and
hematologic
abnormalities
(myelosuppression,
thrombocytopenia,
neutropenia, anemia,
pancytopenia) (mostly
adult reports). Rapid
intravenous
administration has
been associated with
bradycardia and
hypotension. Increased
risk of C. difficile and
other enteric infections
(pediatric and adult
reports).
Cimetidine is a
moderate inhibitor of
CYP metabolism and
can increase levels of
some co-administered
medications, such as
theophylline, SSRIs,
warfarin, and cisapride.
For specific interactions,
refer to the drug
interactions program
included with
UpToDate.
Famotidine Children: Similar to cimetidine, Tablets may be
1 mg/kg per day, except that famotidine crushed (10, 20, and
divided into 2 lacks anti-androgenic 40 mg)
doses § activity (gynecomastia) Flavored powder for
Adults: and does not inhibit suspension (40 mg/5
 20 mg/dose twice CYP metabolism or alter mL)
daily co-administered drugs Intravenous
metabolized by CYP * . formulation
available ¥
Chewable tablets (10
mg, with antacid
[calcium carbonate-
magnesium hydroxide
antacid])
Nizatidine Children: Similar to cimetidine, Oral tablets may be
10 mg/kg/day except that nizatidine crushed (150 and 300
divided into 2 lacks anti-androgenic mg)
doses § activity (gynecomastia) Flavored oral solution
Adults: and does not inhibit (15 mg/mL)
CYP metabolism or alter
150 mg/dose twice
co-administered drugs
daily or 300 mg
metabolized by CYP * .
once daily at
bedtime Low levels of NDMA
contaminants have
been found in some
nizatidine products † .

Prokinetics ‡
Cisapride ** Children: Cisapride is not Restricted availability
0.6 to 0.8 mg/kg per available in the United in the United States **
day, divided into 4 States. The only way
doses, given 30 that United States
minutes before each clinicians can obtain
meal and at bedtime cisapride is through a
Maximum 10 mg limited-access program
per dose developed by Janssen
Pharmaceuticals and
Adults:
the United States
5 to 20 mg 4 times FDA ** .
daily
Frequent:
Abdominal pain,
diarrhea, headache,
dizziness.
Infrequent or rare:
NOTE – Cisapride
may increase the
risk for potentially
fatal ventricular
 arrhythmias due to
QT prolongation.
NOTE – If
prescribed, requires
assessment of risk
factors for cardiac
arrhythmias,
including ECG and
serum
electrolytes ¶¶ and
close attention to
avoiding co-
administration of
drugs that can
elevate cisapride
blood levels and/or
also prolong the QT
interval, including
macrolide
antibiotics, azole
antifungals, and
protease inhibitors.
For specific
interactions, refer to
the drug
interactions
program included
with UpToDate.
Hypersensitivity
reactions (rash,
bronchospasm),
convulsions,
dystonic reactions
(mostly adult
reports).

C. difficile: Clostridioides (formerly Clostridium) difficile; CNS: central nervous system; CYP: cytochrome
P450; ECG: electrocardiogram; FDA: Food and Drug Administration; GERD: gastroesophageal reflux
disease; H2RA: histamine2 receptor antagonist; NDMA: n-nitrosodimethylamine; NG: nasogastric; PPI:
proton pump inhibitor; SSRI: selective serotonin reuptake inhibitor.
* For additional information about adverse effects, refer to separate UpToDate topic reviews of proton
pump inhibitors in the treatment of acid-related disorders and the pharmacology of antiulcer
medications. Additional information is available in the individual drug topics included within UpToDate.
¶ Preparations shown in the table are those available in the United States and some other countries.
Δ Acid suppression with PPIs or H2RAs may be a risk factor for lower respiratory tract infections,
particularly in infants and young children.
◊ Relative potency varies among PPIs. Bioequivalent doses for acid suppression are pantoprazole 0.23,
lansoprazole 0.9, omeprazole 1.0, esomeprazole 1.6, and rabeprazole 1.8 [4] .
§ In general, the pediatric dose should not exceed the higher end of the adult dose. On a milligram per
kilogram basis, doses of some of the PPIs needed to obtain a similar degree of acid suppression in
children are greater than those for adolescents and adults. Optimally, PPIs are given once daily
approximately 30 minutes before the first meal of the day, or if given twice daily, prior to the first meal
and the evening meal.
¥ Intravenous formulations are available for some PPIs and H2RAs and may be used when oral therapy is
inappropriate or not possible (eg, patients in intensive care for stress ulcer prophylaxis). Further
information on intravenous preparations and dosing is available in the individual drug topics included
within UpToDate.
‡ Dose adjustment of H2RAs is needed in the setting of kidney function impairment.
† Ranitidine (an H2RA) was withdrawn from the market in the United States in April 2020 due to concerns
about contamination of some ranitidine products with N-Nitrosodimethylamine (NDMA), a probable
human carcinogen [5] . The NDMA concentrations increase over time, especially when stored at higher
than room temperatures.
** In the United States, prescriptions for cisapride can only be filled through an investigational limited-
access program from the manufacturer, after providing documentation of the need for cisapride and
assessment of risk factors for cardiac arrhythmias in the individual patient (eg, a QTc >450 ms). Cisapride
is available in several other countries. Refer to UpToDate topic on acquired long QT syndrome for details.
¶¶ Systematic reviews have not supported the use of metoclopramide, cisapride, erythromycin, or
domperidone for treatment of GERD. These drugs should be considered for use only in carefully selected
patients who have delayed gastric emptying because of gastric dysmotility (gastroparesis), contributing
to GERD. Refer to the UpToDate topic on treatment of gastroparesis.

Data from:
1. Lightdale JR, Gremse DA and the section on Gastroenterology, Hepatology and Nutrition. Gastroesophageal reflux:
Management guidance for the pediatrician. Pediatrics 2013; 131:e1684.
2. Vandenplas Y, Rudolph D, et al. Guías de práctica clínica para el reflujo gastroesofágico pediátrico: Recomendaciones
conjuntas de la Sociedad Norteamericana de Gastroenterología, Hepatología y Nutrición Pediátricas (NASPGHAN) y la
Sociedad Europea de Gastroenterología, Hepatología y Nutrición Pediátricas (ESPGHAN). J Pediatr Gastroenterol Nutr 2009;
49:498.
3. Rosen R, Vandenplas Y, Singendonk M, et al. Guías de práctica clínica para el reflujo gastroesofágico pediátrico:
Recomendaciones conjuntas de la Sociedad Norteamericana de Gastroenterología, Hepatología y Nutrición Pediátricas
(NASPGHAN) y la Sociedad Europea de Gastroenterología, Hepatología y Nutrición Pediátricas (ESPGHAN). J Pediatr
Gastroenterol Nutr 2018.
4. Kirchheiner J, Glatt S, Fuhr U, et al. Potencia relativa de los inhibidores de la bomba de protones: comparación de sus
efectos sobre el pH intragástrico. Eur J Clin Pharmacol 2009; 65:19.
5. La FDA solicita la retirada del mercado de todos los productos de ranitidina (Zantac). Administración de Alimentos y
Medicamentos de EE. UU. (FDA). Disponible en: https://www.fda.gov/news-events/press-announcements/fda-requests-
removal-all-ranitidine-products-zantac-market (Consultado el 7 de abril de 2020).

Gráfico 55435 Versión 26.0

Cirugía de laringomalacia

(A) Laringoscopia rígida de laringomalacia con tejido supraglótico redundante que oculta las cuerdas
vocales.
(B) Laringoscopia rígida de laringomalacia después de la resección de tejido redundante de la epiglotis y
aritenoides.

Cortesía de Glenn C Isaacson, MD, FAAP, FACS.

Gráfico 56479 Versión 2.0

Divulgaciones de los colaboradores
Dana M. Thompson, MD, MS, MBA, FACS: No existen relaciones financieras relevantes con empresas no
elegibles para declarar. Taher Valika, MD: Otros intereses financieros: Nova Science Publishers [Regalías
de libros de texto]. Todas las relaciones financieras relevantes mencionadas se han mitigado. Glenn C.
Isaacson, MD, FAAP: No existen relaciones financieras relevantes con empresas no elegibles para
declarar. Carrie Armsby, MD, MPH: No existen relaciones financieras relevantes con empresas no
elegibles para declarar.

El grupo editorial revisa las declaraciones de los colaboradores para detectar posibles conflictos de
intereses. De detectarse, se abordan mediante un proceso de revisión multinivel y mediante la exigencia
de proporcionar referencias que respalden el contenido. Todos los autores deben proporcionar contenido
debidamente referenciado y cumplir con los estándares de evidencia de UpToDate.

Política de conflicto de intereses